G. Prinianakis
University of Crete
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Featured researches published by G. Prinianakis.
European Respiratory Journal | 2002
Eumorfia Kondili; G. Prinianakis; H. Athanasakis; Dimitrios Georgopoulos
The pattern of lung emptying was studied in 10 mechanically-ventilated patients with acute respiratory distress syndrome. At four levels of positive end-expiratory pressure (PEEP) (0, 5, 10 and 15 cmH2O) tracheal (Ptr) and airway pressures (Paw), flow (V′) and volume (V) were continuously recorded. Tidal volume was set between 0.5–0.6 L and V′/V curves during passive expiration were obtained. Expired volume was divided into five equal volume slices and the time constant (τe) and effective deflation compliance (Crseff) of each slice was calculated by regression analysis of V/V′ and postocclusion V/Ptr relationships, respectively. In each slice, the presence or absence of flow limitation was examined by comparing V′/V curves with and without decreasing Paw. For a given slice, total expiratory resistance (Rtot) (consisting of the respiratory system (Rrs), endotracheal tube (Rtube) and ventilator circuit (Rvent)) was calculated as the τe/Crseff ratio. In the absence of flow limitation Rrs was obtained by subtracting Rtube and Rvent from Rtot, while in the presence of flow limitation Rrs equaled Rtot. The τe of the pure respiratory system (τers) was calculated as the product of Rrs and Crseff. At zero PEEP, τers increased significantly towards the end of expiration (52±31%) due to a significant increase in Rrs (46±36%). Application of PEEP significantly decreased Rrs at the end of expiration and resulted in a faster and relatively constant rate of lung emptying. In conclusion, without positive end-expiratory pressure the respiratory system in patients with acute respiratory distress syndrome deflates with a rate that progressively decreases, due to a considerable increase in expiratory resistance at low lung volumes. Application of positive end-expiratory pressure decreases the expiratory resistance, probably by preventing airway closure, and as a result modifies the pattern of lung emptying.
Intensive Care Medicine | 2000
K. Valassiadou; G. Prinianakis; E. Sanidas; D. Tsiftsis; Dimitris Georgopoulos
1. Grimmett WG, Dzendolet I, Whyte I (1996) Intravenous thiodan (30% endosulfan in xylene). J Toxicol Clin Toxicol 34 (4): 447±452 2. Dull WL (1988) Treatment of adult respiratory distress syndrome. Drug Intelligence Clin Pharm 22 (5): 402±404 3. Neeld EM, Limacher MC (1978) Chemical pneumonitis after the intravenous injection of hydrocarbon. Radiology. 129 (1): 36 4. Lyon J, Taylor H, Ackerman B (1987) A case report of intravenous malathion injection with determination of serum halflife. Clin Toxicol 25 (3): 243±249 5. Low PS, Ngiam TE, Quak SH (1980) Insecticide Baygon aerosol poisoning ± a report of 5 cases. J Singapore Paediatr Soc 22 (1±4): 44±49
Intensive Care Medicine | 2004
G. Prinianakis; Eumorfia Kondili; Dimitrios Georgopoulos
frequency [3, 4]. The authors correctly observed (using indirect data from our paper) that in the study of Prinianakis et al. [1] expiratory asynchrony increased progressively with increasing pressure support. Indeed, we calculated the actual time that mechanical inspiration extended into neural expiration (Text, an index of expiratory asynchrony), and found that independent of the method of cycling Text increased progressively with increasing PS, averaging 210 ms, 290 ms, and 680 ms with the traditional method of cycling (25% of peak inspiratory flow) and 200 ms, 290 ms, and 710 ms with the flow waveform method of cycling, respectively, during low, moderate and high levels of pressure support. The method of cycling did not influence the magnitude of expiratory asynchrony. Notwithstanding that in the study of Prinianakis et al. [1] chemical feedback was not taken into account these data reconfirmed our previous findings [3, 4]. We certainly agree with the mechanism of expiratory asynchrony discussed by Dr. Mojoli and Dr. Braschi. Indeed, we observed that at least in sedated critically ill patients increasing pressure support is not associated with increased expiratory muscle activity [1, 3, 4], exaggerating the phenomenon of expiratory asynchrony as Dr. Mojoli and Dr. Braschi correctly stated. Nevertheless, another mechanism may be of importance. We have shown that increasing pressure support by augmenting inspiratory flow decreases neural inspiratory time, thus lengthening Text [1, 3, 4]. It follows that increasing pressure support may increase expiratory asynchrony by affecting neural inspiratory time. Collectively, these observations indicate that expiratory asynchrony during pressure support ventilation is due to multiple factors related both to patient and ventilator. We agree, however, with Dr. Mojoli and Dr. Braschi that the clinical impact of this expiratory asynchrony needs further study. References
BJA: British Journal of Anaesthesia | 2003
Eumorfia Kondili; G. Prinianakis; Dimitris Georgopoulos
Journal of Advanced Nursing | 2009
Stella Anifantaki; G. Prinianakis; Efsevia Vitsaksaki; Victoria Katsouli; Stella Mari; Antonios Symianakis; Georgia Tassouli; Eleni Tsaka; Dimitris Georgopoulos
Intensive Care Medicine | 2007
Christina Alexopoulou; Eumorfia Kondili; E. Vakouti; Maria Klimathianaki; G. Prinianakis; Dimitris Georgopoulos
European Respiratory Journal | 2000
Eleni Mouloudi; G. Prinianakis; Eumorfia Kondili; Dimitrios Georgopoulos
Respiratory Care Clinics of North America | 2005
G. Prinianakis; Eumorfia Kondili; Dimitris Georgopoulos
Intensive Care Medicine | 2001
E. Mouloudi; G. Prinianakis; Eumorfia Kondili; Dimitrios Georgopoulos
Respiratory Medicine | 2007
Polychronis Malliotakis; Eleni Mouloudi; G. Prinianakis; Eumorfia Kondili; Dimitris Georgopoulos